Title : Regulation of GABA Neurotransmission by Glutamic Acid Decarboxylase (GAD).

Pub. Date : 2015

PMID : 26377650






7 Functional Relationships(s)
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1 Regulation of GABA Neurotransmission by Glutamic Acid Decarboxylase (GAD). gamma-Aminobutyric Acid glutamate decarboxylase 1 Homo sapiens
2 Regulation of GABA Neurotransmission by Glutamic Acid Decarboxylase (GAD). gamma-Aminobutyric Acid glutamate decarboxylase 1 Homo sapiens
3 Control of GABA neurotransmission at the pre-synaptic site occurs substantially through the activation of the glutamic acid decarboxylase (GAD) enzymes GAD65 and GAD67. gamma-Aminobutyric Acid glutamate decarboxylase 1 Homo sapiens
4 Control of GABA neurotransmission at the pre-synaptic site occurs substantially through the activation of the glutamic acid decarboxylase (GAD) enzymes GAD65 and GAD67. gamma-Aminobutyric Acid glutamate decarboxylase 1 Homo sapiens
5 Control of GABA neurotransmission at the pre-synaptic site occurs substantially through the activation of the glutamic acid decarboxylase (GAD) enzymes GAD65 and GAD67. gamma-Aminobutyric Acid glutamate decarboxylase 1 Homo sapiens
6 GABA neurotransmission is dependent upon whether GAD is associated with synaptic vesicles (SV) and calpain performs a vital role by generating the highly active tGAD65 resulting in augmented GABA synthesis and wrapping uptake into SV. gamma-Aminobutyric Acid glutamate decarboxylase 1 Homo sapiens
7 From studies on a rodent stroke model calpain-mediated cleavage of GAD enzyme has been shown to occur under pathological conditions resulting in less SV refilling and depletion of existing pools of SV releasable GABA. gamma-Aminobutyric Acid glutamate decarboxylase 1 Homo sapiens